Simplified direct Fick techniques for measurement of cardiac output in seriously ill patients

Simplified direct Fick techniques for measurement cardiac output in seriously ill patients M. G. M. E.

of

M. Scheinman, M.D. T. Evans, M.D. A. Brown, M.D. Rapaport, M.D. San Francisco, Calif.

I

ntelligent management of the seriously ill cardiac patient is facilitated when accurate measurements of systemic flow are available to the clinician.‘s2 Cardiac output is generally determined either by the direct Fick method3 or by dye dilution techniques4 Both methods have been used successfully in the cardiac catheterization laboratory but they have practical limitations when applied to critically ill patients. The direct Fick method requires pulmonary artery catheterization for obtaining mixed venous blood and facilities for measuring oxygen consumption and the oxygen content of blood samples. The dye dilution technique requires a densitometer and recording equipment as well as trained technical support; furthermore, it may give falsely low cardiac output values in patients with severe low-output states.5 These considerations have discouraged widespread application of either method except in research programs. The present report describes some experimental results allowing for practical modification of the direct Fick method for measuring cardiac output in critically ill subjects.

Materials

and

methods

Thirty-seven cardiac patients were studied over a two-year period (1967 to 1969) in an intensive coronary care unit. A small nylon catheter was inserted percutaneously into a medial antecubital vein and flow directed into the pulmonary artery by means of a technique described previously.6 A polyethylene central venous catheter was inserted percutaneously into the antecubital, external jugular, or subclavian vein and passed into the right atrium under electrocardiographic monitoring.’ The catheter was filled with 3 per cent sodium chloride and closed off with a metal stopcock. One end of an alligator clamp was connected to the stopcock and the other end to the unipolar chest lead cable with other leads attached to the patient and the electrocardiograph selector switch in the V position. The catheter was advanced until a typical atria1 electrogram from the superior portion of the right atrium was obtained, i.e., deeply inverted “P” waves, and then advanced further for one or two inches. The “P” waves were usually diphasic in this catheter position. Catheter

From

the Cardiopulmonary Laboratow and Medical Services, San Francisco General Hospital, and the Department of Medicine and the Cardiovascular Research Institute, University of California, San Francisco, Calif. This work was supported in part by United States Public Health Service Grant HE-06285 Received for publication March 31, 1971. Reprint requests to: Melvin Scheinman, M.D., Regional Medical Programs, Room 3501. San Francisco General Hospital, 1001 Potrero Ave., San Francisco, Calif. 94110.

Vol. 83, No. 1, ffi. 61-66

January, 1972

American Heart Journal

61

62

Am. Heart I. January, 1972

Scheinman et al.

RIGHT ATRIA1

Fig.

1. Comparison

of right

atrial

OXYGEN

and pulmonary

localization at the mid or upper (usually lateral edge) part of the atrium was confirmed by roentgenography in all patients. The fluid in the catheters in the right atrium and pulmonary artery was aspirated and 3 C.C. of blood was then withdrawn simultaneously from both catheters for immediate oximetric analysis of oxygen saturation (A-O oximeter). A nose clamp was applied to 13 subjects who breathed through a low-resistance J valve into either a basal metabulator or a Douglas bag. Oxygen consumption was determined by either analysis of the slope of the basal metabulator tracing or direct analysis of expired gases,using a Beckman Model C Gas Analyzer. In these 13 subjects oxygen consumption was measured sequentially first by direct analysis of expired gases and finally by the basal metabulator. Six of these patients needed mechanical ventilatory support via an endotracheal tube and the metabulator was connected directly to the tube. Control pulmonary artery oxygen saturation was measured in 17 patients breathing room air who had severe heart failure

% SATURATION

artery

oxygen

saturation

in 37 patients.

and/or shock. Serial pulmonary artery blood samples were then analyzed at one, two, four, six, eight, and ten minutes while the patients were rebreathing 100 per cent oxygen from the basal metabulator. In five patients who breathed 100 per cent oxygen for 30 minutes, serial tenminute samples showed no statistically significant difference between the per cent of pulmonary artery oxygen saturation at 30 and 10 minutes. Hence, the value after 10 minutes was used as the maximal mixed venous oxygen saturation with oxygen breathing. Results

Eighty-four simultaneous determinations of right atria1 and pulmonary artery saturations were obtained. The clinical diagnosis and data are summarized in Table I and Fig. 1. There was no statistically significant difference and correlation between right atria1 and pulmonary artery oxygen saturation was excellent with a correlation coefficient (Y) = +0.97 (Fig. 1). The data for the I7 patients in severe heart failure and/or shock studied during

Volume Number

83

of cardiac outfiut

Measurement

1

63

. :

. --a---5--

8

I+-

. .

: :

8

*

.

--T--

:

80-

.

70-

.

60-

: ,ol

ROOM

BASAL AIR

i 1

I 2 TIME

!

METABULATOR-, I 4

I 6

I 8

I 10

IN MINUTES

Fig. 2. Pulmonary artery oxygen saturation curves in 17 patients breathing via a basal metabulator. The 10 minute value for each patient is taken as maximal mixed venous oxygen saturation and expressed as 100 per cent; all other values are expressed as per cent of the maximal value. The straight heavy lines represent mean values for each time period while the dashed line represents the standard deviation for the mean.

oxygen breathing are summarized in Table II. Ninety-seven per cent of maximal mixed venous oxygen saturation was achieved in the two-minute sample and saturation was complete by the fourth minute (Fig. 2). There was no statistically significant difference between pulmonary artery oxygen saturations at two, four, six, eight, and ten minutes. Results of the two methods for measuring oxygen consumption are compared in Fig. 3. There was no statistically significant difference between the two techniques and the average difference was approximately 12 per cent. The central venous catheter was left in place for as long as six days in four patients to allow serial measurement of right atria1 oxygen saturation. In three patients an atria1 injury current and atria1 premature beats were noted as the catheter was advanced into the atrium. These abnormalities disappeared when the catheter was repositioned. In one patient a transient bout of atria1 fibrillation that persisted for approximately two hours occurred after removal of the catheter. No pulmonary emboli, sepsis, or death resulted from this procedure.

Table I. Diagnosis and number of studies in patients in whom simultaneous right atria1 and pulmonary artery oxygen

saturations were obtained

Diagnosis Cardiogenic shock Heart failure Hemorrhagic shock Pulmonary embolus Sepsis Cerebrovascular accident Barbiturate overdose Hepatorenal syndrome Total

I

No. of patients 9 9 3 4 5 4 2 1

37

I

No. of determinations 26 24 6 10 6 8 2 1 84

Discussion

Prior studies in man generally showed good agreement between right atria1 and mixed venous oxygen contents at the time of cardiac catheterization, especially if the atria1 catheter was positioned just above the tricuspid valve. *,QHowever, Shore and associates*Oobserved a wide divergence in the oxygen content of two blood samples

64

Am. Heart J. January, 1972

Scheinman et al.

Table II. Serial measurements of pulmonary after breathing via a basal metabulator

artery oxygen saturation

Pulmonary

artery oxygen ~~--~--~_--

i------------__ Diagnosis

After breathing __---__-~___-___

Before -2 I Acute myocardial with shock

4

58 64.7 38.5 59 40

61 66 62.2 58 47

67.5 69.5 69.5 61.2 52

68 73.2 72.5 65 55

Acute myocardial infarction with heart failure and shock

62.3 52

49

68.2 53

Acute myocardial infarction with shock and congestive heart failure

34

35.5

Acute myocardial with congestive

68 62

saturation

via basal

/

6

(To)

metabulator

/

8

(min.)

/

10

/ 20*

/ 30*

74 66 61

70.5 75.5 70 65 65

70.8 75 66.2 60

-

-

69 -

67 -.-

65.5 52.5

64.8 51

66.5 56

65.0 57

66 59

67 56

36.2

38

36

42.4

42.4

44

40

71 69

75 71

76 71

78 72

76.5 73

76.5 72

78 -

76.5 -.

46

74

77

85

79

84

85

Hypertensive cardiovascular disease with congestive heart failure

75 62.7

74 76.8

82 79.7

81 75.8

81 77.4

80 76.8

82 75.0

-

-

Ischemic heart disease with congestive heart failure

75 73 62.7

77 77.5 76.8

78 80.5 79.2

80 80.0 75.8

79.8 81 77.4

83 80.5 76.8

82 81 75

Mitral valve congestive

71.5

73.5

74.5

75

76

71

69

-

-

Septic

*The

infarction

1

l

in 17 patients before and

infarction heart failure

shock

20 and

disease with heart failure

30 minute

samples

were

obtained

from

patients

breathing

obtained simultaneously from either two points in the right atrium or the right atrium and ventricle. Similarly, Warren and associate@ found occasional wide divergence between right atria1 and right ventricular oxygen content. We are unaware of any previous studies comparing right atria1 and mixed venous oxygen content in critically ill cardiac patients at the bedside prior to our own previously reported small series at the time we looked at central venous oxygen saturation.12 Our present data indicate that in these critically ill patients the middle and upper portions of the right atrium serve as an excellent mixing chamber for systemic venous return as evidenced by the excellent correlations

100 per cent

oxygen

for this

period.

found between right atria1 and pulmonary artery oxygen saturations. Furthermore, right atria1 catheterization using a standard central venous catheter may be readily and safely performed even in critically ill patients by advancing the saline-filled catheter under electrocardiographic monitoring into the atrium. Using this technique and advancing the catheter for one to two inches after the typical atria1 electrogram was obtained, we were subsequently able to localize the position of the catheter in the mid to upper portions of the right atrium in all subjects. It is obviously important that the catheter not be positioned in close proximity to the coronary sinus since its very low oxygen

Volunze Number

83 1

saturation is apt to result in a right atria1 oxygen saturation that underestimates true mixed venous oxygen saturation. Likewise, the oxygen saturation of blood from the superior vena cava is an invalid measure of pulmonary artery oxygen saturation since it tends to be higher than true mixed venous oxygen saturation in patients with shock and severe heart failure.i2 Others have emphasized the value of following serial central venous oxygen saturations in patients with acute myocardial infarction.13J4 The right atria1 oxygen saturation provides an even better index of cardiac output since it correlates so well with pulmonary artery oxygen saturation. Finally, right atria1 oxygen content allows quantitation of right to left shunts15 as well as direct measurement of cardiac output if oxygen consumption and arterial oxygen content are also obtained. It must be appreciated that the oximeter measures oxygen saturation and not oxygen dissolved in the plasma; hence, the arterial oxygen content should be measured either directly (e.g., method of Van Slyke and Neil’” or by adding the dissolved oxygen (estimated from the arterial POT and pH) to the blood oxygen capacity (estimated from measurement of hemoglobin concentration). We have found that the basal metabulator allows for rapid, convenient, and accurate measurement of oxygen consumption. Steady-state maximal mixed venous oxygen content is achieved within minutes after breathing 100 per cent oxygen even in patients with severe low-output states. The significant rise in mixed venous oxygen saturation noted after oxygen breathing is most likely due to increased dissolved oxygen in plasma rather than to increased cardiac output. Although serial cardiac outputs were not measured in the present study, others have shown a tendency for the cardiac output to remain unchanged or fall with oxygen breathing.17,** The technique is quickly mastered by the uninitiated and well tolerated by severely ill patients. Obvious leaks that might occur from a malpositioned mouthpiece or an incompletely occlusive endotracheal tube are readily evident from the spirometric trace and allow the operator to institute immediate corrective measures. Theoretically, hyperventilation or sud-

Measurement

of cardiac output

65

400 r 35oc

loo00 BASAL

Fig. 3. Comparison nique with analysis oxygen consumption.

METABULATOR

of the basal metabulator techof expired gases for measuring

den increases in total lung volume during measurement of oxygen consumption would result in a falsely high value.ig This error should be further magnified when breathing 100 per cent oxygen and using the basal metabulator as opposed to breathing room air and analyzing the expired gases. In practice, however, we found excellent correlation between the two methods. The average difference was 12 per cent in the 13 subjects studied. Furthermore, we showed that a steady state is rapidly achieved and maximal mixed venous oxygen saturation occurs within minutes even in patients with shock or severe left ventricular failure when placed on 100 per cent oxygen. Serial monitoring of flow is of obvious benefit in assessing circulatory impairment as well as in evaluating the effects of various therapeutic maneuvers in seriously ill cardiac patients. Unfortunately, present techniques are time consuming and necessitate use of expensive equipment and/or skilled technical support, thus precluding widespread acceptance. Our own study shows that valid measurements of cardiac outputs can easily be obtained by the direct Fick method with equipment readily available in most hospitals. Furthermore, valu-

66

Am. Heart J. January, 1972

Scheinman et al.

able hemodynamic information without harm to the patient.

is obtained

Summary

Eighty-four simultaneous determinations of right atria1 and pulmonary artery oxygen saturations were performed in 37 patients in a coronary care unit. Correlation between right atria1 and pulmonary artery oxygen saturations was excellent (r = +0.97). Pulmonary artery oxygen saturation curves were determined in 17 patients with heart failure and/or shock while breathing 100 per cent oxygen via a basal metabulator. Maximal mixed venous oxygen saturation was achieved within two minutes in all patients. Oxygen consumption was measured by both basal metabulator and direct analyses of expired gasesin 13 subjects. Values for oxygen consumption measured by the two methods correlated well (r = $0.897). Use of right atria1 oxygen content from a central venous catheter combined with arterial blood samples from an indwelling catheter and oxygen consumption obtained from the basal metabulator simplifies measuring cardiac output by the direct Fick method in severely ill patients and permits serial measurements to follow results of therapeutic interventions.

REFERENCES Rapaport, E., and Scheinman, M. M.: Rationale and limitations of hemodynamic measurementsin patients with acute myocardial infarction, Mod. Concepts Cardiovc. Dis. 3855, 1969. Talley, R. C., Goldberg, L. I., Johnson, C. E., and McNay, J. L.: A hemodynamic comparison of dopamine and isoproterenol in patients in shock, Circulation 39:361, 1969. Klein, 0.: Zur Bestimmung dir zirkulatorishen Minuten volumens beim Menschen nach dem Fickschen Prinzip (Gewinnung des gemischten venosen Blutes mittels Herzsondierung), Munch. Med. Wochenschr. 77:1311, 1930. Sleeper, J. C., Thompson, H. K., Jr., McIntosh, H. 0.. and Elston. R. C.: Reoroducibilitv , of results obtained with indicator-dilution technique for estimating cardiac output in man, Circ. Res. 11:712, 1962.

5. Smith, H. J,, Oriol, A., March, J., and McGregor, M.: Hemodynamic studies in cardiogenie shock. Treatment with isoproterenol and metaraminol, Circulation 35:1084, 1967. 6. Scheinman, M. M., Abbott, J. A., and Rapaport, E.: Clinical uses of a flow-directed right heart catheter, Arch. Intern. Med. 124:19, 1969. M. C.: Technique for obtaining accu7. Robson, rate reproducible central venous pressure, Johns Hopkins Med. J. 122:232, 1968. 8. Cournand, A., Riley, R. L., Breed, E. S., Baldwin, E. D., and Richards, D. W., Jr.: Measurement of cardiac output in man using the technique of catheterization of the right auricle or ventricle, I. Clin. Invest. 24:106. 1945. 9. Barrat-Bo;es, B. G., and Wood, E. H.: The oxygen saturation of blood in the venae cavae, right-heart chambers, and pulmonary vessels of healthv subiects. I. Lab. Clin. Med. 50:93. 1957. ” 10. Shore, R., Holt, J. P., and Knoefel, P. K.: Determination of cardiac output in the dog by the Fick procedure, Am. J. Physiol. 143:709, 1945. 11. Warren, J. V., Stead, E. A., Jr., and Brannon, E. S.: Cardiac output in man; a study of some of the errors in the method of right heart catheterization, Am. J. Physiol. 1455458, 1946. 12. Scheinman, M. M., Brown, M. A., and Rapaport, E.: Critical assessment of use of central venous oxygen saturation as a mirror of mixed venous oxygen in severely ill cardiac patients, Circulation 40:165, 1969. 13. Goldman, R. H., Braniff, B., Harrison, D. C., and Spivack, A. D.: Use of central venous oxygen saturation measurements in a coronary care unit, Ann. Intern, Med. 68:1280, 1968. 14. Hutter, A. M., Jr., and Moss, A. J.: Value of serial central venous oxygen saturations in acute myocardial infarction, Circulation 38 (Suppl. VI):VI-104, 1968. 1.5. Comroe, J. H., Forster, R. E., Dubois, A. B., Briscoe, W. A., and Carlsen, E.: The Lung, Ed. 2. Chicago. 1962. Year Book Medical Publishers, Inc.,p.’ 343. ’ 16. Van Slyke, D. D., and Neil, J. M.: Determination of gases in blood and other solutions by vacuum extraction and manometric measurement, J. Biol. Chem. 61:523, 1924. 17. Kenmure, A. C. F., Murdoch, W. R., Beattie, A. D., Marshall, J. C. B., and Cameron, A. J. V.: Circulatory and metabolic effects of oxygen in myocardial infarction, Br. Med. J. 4:360, 1968. 18. Foster, G. L., Casten, G. G., and-Reeves, T. J.: The effects of oxygen breathing in oatients with acute myocardial infarction, Cardiovasc. Res. 3:179, 1969. 19. Guyton, A. C.: Circulatory Physiology: Cardiac Output and Its Regulation, Philadelphia, 1963, W. B. Saunders Company, p. 36. .I